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Aryl hydrocarbon hydroxylase tissue-specific activities: evidence for baseline levels in mammalian tissues
Abstract:
The tissue-specific activities (units per gram tissue) of arylhydrocarbon hydroxylase benzo[a]pyrene [AHH(BaP)] (EC 1.14.14.2) in human, mouse, rat, and hamster have been reviewed. Three categories of AHH activities are defined: baseline values from tissues that have been protected from adventitious exposures to AHH inducers; background levels from tissues where there have been no overt measures to protect against exposure; and induced levels resulting from overt exposure to chemical inducers. Evidence that the baseline category exists is derived from the observations that an upper limit of AHH tissue-specific activity of about 1.5 nmol/h . g tissue occurs in human placenta, human foreskin, lymphocyte, and epitheliod and fibroblastoid cell lines; mouse lung and liver; rat fetal liver, and noninducible rat cell lines from lung, liver, embryo kidney, and adrenals; and hamster kidney. The collected values for nonexposed tissues range from 0.02 nmol/h . g to values less than 1.5 nmol/h . g. The most consistent observation of this type was from human placental material from nonsmoking mothers. Animals raised under standard laboratory conditions without special dietary precautions show background AHH activities that range from 2 nmol/h . g to 200 nmol/h . g in portal of entry tissues such as liver, lung, and intestines. Almost all tissue samples showed induced AHH levels of up to 500 nmol/h . g when those tissues were overtly exposed to substances containing chemical inducers of AHH. Measurements of placental AHH from smoking mothers showed that more than 95% of those samples had AHH values exceeding 2.5 nmol/h . g. This natural bimodal distribution of AHH activities, across species and in different tissues, of baseline values of less than 1.5 nmol/h . g and background or induced AHH activities with values greater than 1.5 nmol/h . g, may provide a reference set of values for use in quantification of the role of AHH in the induction of disease.